Affiliation: Tufts University
- Chaperone-mediated autophagyJ Fred Dice
Department of Cellular and Molecular Physiology, Tufts University School of Medicine, Boston, MA 02111, USA
Autophagy 3:295-9. 2007..These findings reveal a rich complexity of mechanisms to control CMA activity...
- Mechanisms of chaperone-mediated autophagyAmy E Majeski
Department of Physiology, Sackler School of Graduate Biomedical Sciences, Tufts University School of Medicine, 136 Harrison Avenue, Boston, MA 02111, USA
Int J Biochem Cell Biol 36:2435-44. 2004..The exact roles of this lysosomal chaperone remain to be defined. The mechanisms of chaperone-mediated autophagy are similar to mechanisms of protein import into mitochondria, chloroplasts, and the endoplasmic reticulum...
- Ketone bodies stimulate chaperone-mediated autophagyPatrick F Finn
Department of Molecular and Cellular Physiology, Tufts University School of Medicine, Boston, Massachusetts 02111, USA
J Biol Chem 280:25864-70. 2005..The induction of CMA by ketone bodies may provide an important physiological mechanism for the activation of CMA during prolonged starvation...
- Effects of small molecules on chaperone-mediated autophagyPatrick F Finn
Department of Cellular and Molecular Physiology, Tufts University School of Medicine, Boston, Massachusetts 02111, USA
Autophagy 1:141-5. 2005..Finally we demonstrate that the glucose-6-phophate dehydrogenase inhibitor, 6-aminonicotinamide, and heat shock protein of 90 kilodaltons inhibitor, geldanamycin, have the ability to activate CMA...
- Proteolytic and lipolytic responses to starvationPatrick F Finn
Department of Molecular and Cellular Physiology, Tufts University School of Medicine, Boston, Massachusetts, USA
Nutrition 22:830-44. 2006..Tissues that cannot use ketone bodies for energy respond to these small molecules by activating chaperone-mediated autophagy. This is one form of interaction between proteolytic and lipolytic responses to starvation...
- Chaperone-mediated autophagy is defective in mucolipidosis type IVBhuvarahamurthy Venugopal
Center for Human Genetic Research, Massachusetts General Hospital, Harvard Medical School, Boston, Massachusetts 02114, USA
J Cell Physiol 219:344-53. 2009..It is also possible that TRPML1 channel activity may be required for CMA. Understanding the role of TRPML1 in CMA will undoubtedly help to characterize the pathogenesis of MLIV...
- PROTEIN DEGRADATION IN AGING HUMAN FIBROBLASTSJAMES DICE; Fiscal Year: 2005..These studies will include correction of the receptor levels in lysosomes of aged cells and analysis of the effects of restoring this protein degradation pathway on levels of aberrant proteins in senescent cells. ..